Tumor Necrosis Factor α Gene Expression in Human Peritoneal Macrophages Is Suppressed by Extra-abdominal Trauma

Hauser, Carl J.; Lagoo, Sandhya A.; Lagoo, Anand S.; Hale, Enatra; Hardy, Kenneth J.; Barber, William H.; Bass, J. David; Poole, Galen V.

doi:10.1001/archsurg.1995.01430110044008

Cited by 11 publications

(3 citation statements)

References 9 publications

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“…Polymicrobial sepsis has been found to reduce the capacity of peritoneal macrophages to release proinflammatory cytokines in re- sponse to lipopolysaccharide (45). Clinically, Hauser et al (46) demonstrated that polytrauma significantly reduces TNF-␣ messenger RNA expression in peritoneal macrophages while simultaneously increasing IL-10 messenger RNA in PBMCs. This is even more remarkable because these data are corroborated by our findings of an increased IL-10 production in PBMCs associated with decreased production of proinflammatory mediators in peritoneal macrophages.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge*

Perl

Gebhard²,

Brückner³

et al. 2005

Critical Care Medicine

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Section: Discussionmentioning

confidence: 99%

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge*

Perl

Gebhard²,

Brückner³

et al. 2005

Critical Care Medicine

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“…Anti-inflammatory cytokines (e.g., IL-10 and transforming growth factor beta [TGF-beta]) are involved in the downregulation of the inflammatory response. For instance, IL-10 can deactivate macrophages; and the TNF levels in patients with trauma get higher when IL-10 levels are depressed, a scenario that has been implicated in the onset of septic complications [95]. TGF beta is a potent inhibitor of monocyte activation [96]; and significantly elevated levels of TGF beta have been observed in monocytes derived from immunosuppressed patients after trauma.…”

Section: Comparison Of Systemic Inflammation In Sepsis and Hemorrhagementioning

confidence: 99%

Novel Insights for Systemic Inflammation in Sepsis and Hemorrhage

Cai

Deitch

Ulloa

2010

Mediators of Inflammation

103

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The inflammatory responses in sepsis and hemorrhage remain a major cause of death. Clinically, it is generally accepted that shock in sepsis or hemorrhage differs in its mechanisms. However, the recognition of inflammatory cytokines as a common lethal pathway has become consent. Proinflammatory cytokines such as tumor necrosis factor (TNF) or high-mobility group box1 (HMGB1) are fanatically released and cause lethal multiorgan dysfunction. Inhibition of these cytokines can prevent the inflammatory responses and organ damage. In seeking potential anti-inflammatory strategies, we reported that ethyl pyruvate and alpha7 nicotinic acetylcholine receptor (alpha7nAChR) agonists effectively restrained cytokine production to provide therapeutic benefits in both experimental sepsis and hemorrhage. Here, we review the inflammatory responses and the anti-inflammatory strategies in experimental models of sepsis and hemorrhage, as they may have a consistent inflammatory pathway in spite of their different pathophysiological processes.

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“…15 Another study demonstrated decreased TNF␣ mRNA levels in human peritoneal macrophages after polytrauma, while the antiinflammatory cytokine IL-10 was upregulated. 16 Taken together, these results suggest that the early innate immune response, as well as the adaptive immune response, to pathogens is attenuated in patients with TBI. However, the mechanism underlying this immune paralysis following brain injury remains unclear.…”

Section: Immune Paralysis In Patients With Tbimentioning

confidence: 81%

Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury

Kox¹,

Pompe²,

Pickkers³

et al. 2008

Neurology

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Traumatic brain injury (TBI) is a leading cause of death and disability, especially in the younger population. In the acute phase after TBI, patients are more vulnerable to infection, associated with a decreased immune response in vitro. The cause of this immune paralysis is poorly understood. Apart from other neurologic dysfunction, TBI also results in an increase in vagal activity. Recently, the vagus nerve has been demonstrated to exert an anti-inflammatory effect, termed the cholinergic anti-inflammatory pathway. The anti-inflammatory effects of the vagus nerve are mediated by the ␣7 nicotinic acetylcholine receptor present on macrophages and other cytokineproducing cells. From these observations, we hypothesize that the immune paralysis observed in patients with TBI may, at least in part, result from augmented vagal activity and subsequent sustained effects of the cholinergic anti-inflammatory pathway. This pathway may counteract systemic proinflammation caused by the release of endogenous compounds termed alarmins as a result of tissue trauma. However, sustained activity of this pathway may severely impair the body's ability to combat infection. Since the cholinergic anti-inflammatory pathway can be pharmacologically modulated in humans, it could represent a novel approach to prevent infections in patients with TBI. Neurology

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Tumor Necrosis Factor α Gene Expression in Human Peritoneal Macrophages Is Suppressed by Extra-abdominal Trauma

Abstract: Human PM phi constitutively show high levels of TNF-alpha message expression, and this is down-regulated by polytrauma. This might constitute a functionally "primed" state. If so, TNF-alpha down-regulation might contribute to functional PM phi suppression after systemic injury.

Cited by 11 publications

References 9 publications

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge*

Pulmonary contusion causes impairment of macrophage and lymphocyte immune functions and increases mortality associated with a subsequent septic challenge*

Novel Insights for Systemic Inflammation in Sepsis and Hemorrhage

Increased vagal tone accounts for the observed immune paralysis in patients with traumatic brain injury

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